The major focus of this research is the relation to the neoplastic state of the commonly observed deficiency in tumor tRNA of the modified nucleoside Q. Q is unique because: (1)\it is synthesized at the polynucleotide level by the exchange of Q base with a G in the first position of certain anticodons; (2)\Q base is not synthesized by mammals, but is provided by the diet; and (3)\recent data from our laboratory indicates that animal cells can salvage Q base, enabling its reuse, when tRNA is turned over. We have studied the incorporation of queuine (Q base) into tRNA and its fate upon tRNA turnover in the Vero and L-M cell lines, using the labeled Q base analog [3H]dihydroqueuine. [3H]dihydroqueuine is salvaged from tRNA and reused by Vero cells, but not by L-M cells, which instead accumulate [3H]dihydroqueuine in the culture medium. More recently, again employing [3H]dihydroqueuine and HPLC analysis, we have detected an activity in Vero cell extracts which apparently is responsible for Q-base salvage. This activity converts Q-5'-phosphate, into Q base. Neither Q-3'-phosphate, mannosyl-Q-5'-phosphate, nor Q nucleoside support the reaction. Since exogenous Q nucleoside can be used as a source of Q base by Vero cells, the presence of a kinase which is active with Q nucleoside is implied. Additional support for the existence of such a kinase comes from the slow conversion of Q nucleoside to Q-5'-phosphate in Vero cell extracts. L-M cells lack the Q salvage activity, but apparently retain the kinase activity; Q-5'-phosphate accumulates within L-M cells, but Q base cannot be recovered. The present working hypothesis is that some tumors may be deficient in Q salvage and that Q hypomodification may be a predisposing factor (perhaps one of several factors) for neoplasia.